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作 者:张晓隆[1] 王方岩[1] 徐正祄[1] 王万铁[1] 郝卯林[1]
机构地区:[1]温州医学院病理生理学教研室,浙江温州325035
出 处:《中国应用生理学杂志》2008年第2期161-165,共5页Chinese Journal of Applied Physiology
基 金:浙江省卫生厅科研基金资助项目(SWS00021)
摘 要:目的:探讨红花(safflor injection,SI)抗肺缺血/再灌注损伤作用及其机制。方法:复制在体兔肺缺血/再灌注损伤模型。30只日本大耳兔,随机均分为三组:假手术组(S组),缺血/再灌注组(I/R组)和缺血/再灌注+红花注射液组(SI组)。实验结束时,自颈动脉抽血检测丙二醛(MDA)含量、超氧化物歧化酶(SOD)和黄嘌呤氧化酶(XO)活力。取肺组织测湿干重比(W/D),计算肺泡损伤率(IAR),电镜观察细胞超微结构改变。免疫组化法检测肺组织COX-1、COX-2蛋白表达的变化;组织原位杂交法检测肺组织COX-1mRNA、COX-2mRNA表达的变化。结果:I/R组血清MDA、XO均显著高于S组,SOD明显低于S组(P<0.01);I/R组和SI组的W/D与IAR均高于S组(均P<0.05和P<0.01),SI组显著低于I/R组(P<0.01);I/R组肺组织的超微结构损伤严重,SI组损伤程度明显较轻;免疫组化和原位杂交发现I/R组肺组织COX-2蛋白和COX-2mRNA表达皆显著高于SI组(均P<0.01),肺组织COX-1蛋白和COX-1mRNA表达三组间无明显变化。结论:肺缺血/再灌注损伤可诱导肺组织COX-2的表达,SI可能通过抗氧化应激和下调肺组织COX-2蛋白及其基因的表达而减轻肺缺血/再灌注损伤。Aim: To observe protective effects of saffior injection (SI) on lung ischemia/reperfusion injury (LIRI) and investigate its potential mechanism. Methods: Rabbit lung model of ischemia/reperfusion injury was constituted in vivo. The rabbits were randomly divided into three groups: sham-operation group(S group), ischernia/reperfusion group( IZR group) and ischemia/reperfusion plus safflor injection group (SI group). Malondialdehyde (MDA)content, superoxide dismutase (SOD) and xanthine oxidase(XO) activities in serum were measured. The lung tissue sampled at the end of the experiment was assayed for wet/dry weight ratio (W/D), injured alvcoli rate (IAR) and ultrastructural changes were observed under electron microscope.The expression of COX-1 and COX-2 were measured by immunohistochemistry(IHC). The expressions of COX-lmRNA and COX-2mRNA were observed by in situ hybridization(ISH) .Results: In I/R group, XO and MI)A increased and SOD decreased in serum, while the same changes happened in SI group but less severely(P〈0.01). The value of W/D and IAR was much higher in IZR group than S group, but decreased in SI group. Electron microscope showed obvious ultrastructural injury brought by LIRI in IZR group, which was greatly attenuated in SI group. The IHC and ISH demonstrated that COX-2 and COX-2mRNA in pulmonary tissue of I/R group were significantly higher than those of SI group (P〈0.01). The difference of COX-1 and COX-lmRNA in pulmonary tissue among the three groups was not significant. Conclusion: The ischemia/reperfusion lung injury insults induced the regulation of COX-2 in lung. Safflor injection may attenuate lung ischemia/reperfusion injury through inhibiting cyclooxygenase-2 expression.
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